Neurological disorders, such as neuromotor and neurocognitive disorders including those that are degenerative in nature, can result in significant deterioration of a patient's quality of life. Most neurological disorders can be treated to some extent by medication. In the case of Parkinson's Disease (PD), although anti-parkinsonian medications may improve PD motor function, their effectiveness declines as the disease progresses and disabling dyskinesias often develop after prolonged L-DOPA use. Moreover, many people prefer more natural alternatives to medication.
Some studies have been conducted in animals to determine if exercise can be beneficial in treating PD. (See e.g., Poulton et al., “Treadmill training ameliorates dopamine loss but not behavioral deficits in hemi-Parkinsonian rats,” Experimental Neurology, 193: 181-197 (2005); and Tillerson et al., “Exercise induces behavioral recovery and attenuates neurochemical deficits in rodent models of Parkinson's disease,” Neuroscience, 119: 899-911 (2003)). In fact, animal studies have shown that forced-exercise improves motor function and has neuroprotective qualities. Specifically, in a forced-exercise paradigm, in order to avoid a noxious stimuli, rodents that were injected with 6-hydroxydopamine (6-ODHA) to simulate PD, exercise on a motorized treadmill at a rate greater than their preferred exercise rate.
However, the promising results from animal forced-exercise studies have not been translated to human patients with PD. Different forms of exercise have been used with Parkinson's patients. For example, traditional mechanical therapy activities, performance of sports training, unsupported treadmill walking, partial body weight supported treadmill walking, or a combination of endurance exercise activities have been used to improve PD motor skills. (See e.g., Herman et al., “Six weeks of intensive treadmill training improves gait and quality of life in patients with Parkinson's disease: a pilot study. Arch. Phys. Med. Rehabil., 88:1154-1158 (2007); and Pohl et al., “Immediate effects of speed-dependent treadmill training on gait parameters in early Parkinson's disease,” Arch. Phys. Med. Rehabil., 84: 1760-1766 (2003)). Nonetheless, a meta-analysis concluded that there was insufficient evidence to support the effectiveness of exercise therapy for Parkinson's patients. (See e.g., Smidt et al., “Effectiveness of exercise therapy: A best-evidence summary of systematic reviews,” Aust. J. Physiotherapy, 51:71-85 (2005)).
In addition, the debilitating effects of PD and other neuromotor and neurocognitive disorders typically inhibit people from achieving the full benefits of exercise in treating their respective disorder. In fact, patients with PD produce slow and irregular movements that limit their ability to exercise at the relatively high rates that may be necessary to improve motor function. See e.g. DeLong M R, “Primate models of movement disorders of basal ganglia origin.” Trends in Neuroscience, 13(7): 281-185 (1990); Playford E D et al., “Impaired activation of frontal areas during movement in Parkinson's disease: a PET study,” Adv. Neurol, 60: 506-510 (1993); Playford et al., “Impaired mesial frontal and putamen activation in Parkinson's disease: a positron emission tomography study,” Ann. Neurol., 32(2): 151-161 (1992); and Eidelberg et al., “The metabolic topography of parkinsonism,”Journal of Cerebral Blood Flow and Metabolism, 14: 783-801 (1994)). Furthermore, at later stages of some neurological disorders, including PD, medication can be less effective, thus further impairing a patient's capability to exercise.